臺灣博碩士論文加值系統

背景：糖尿病病患有著較高比例慢性肌肉骨骼疼痛的情形。目的：評估血糖控制對於肌肉骨骼關節疼痛病患進行復健治療效果的影響。方法：針對臨床上有不明的慢性肌肉筋膜疼痛、膝退化性關節炎、肩關節沾黏的疾病，同時合併有血糖值偏高的患者納入本實驗。控制組有4位 （平均年齡68歲；範圍：63-77歲），進行正規的復健儀器治療；而實驗組有6位（平均年齡69歲；範圍：57-88歲），除了正規復健儀器治療外，介入胰島素治療三個月。二組在治療前與後，各抽取血液測量HbA1c、空腹血糖、體內hsCRP、白血球及作VAS視覺疼痛等級(Visual analogue scale)評量。實驗結果：不論實驗組或是控制組，其體內HbA1c經過三個月的復健治療皆顯著降低。HbA1c降低超過0.6者，其VAS疼痛量尺下降的幅度顯著（~3倍）高於其餘的病患，但控制組與胰島素組無顯著的組間差異。二組對於體內的發炎指數hsCRP 及白血球的變化，則無法看出顯著差異。結論：本研究發現HbA1c降低幅度超過0.6者，疼痛復健治療效果明顯較佳。

Background: Diabetes patients are known to have high incident rate of chronic musculoskeletal pain. Purpose: To evaluate the effect of glycemic control on therapeutic efficacy of rehabilitation treating chronic musculoskeletal pain. Method: Diabetes patients having chronic myofascial pain, osteoarthritic knee, or frozen shoulder were included in this study. Four control patients (average age: 68 years; range: 63-77 years) received conventional rehabilitative modality; whereas 6 patients (average age: 69 years; range 57-88 years) with the same rehabilitative modality received daily insulin injection for 3 months. HbA1c, fasting blood glucose, hsCRP, and white blood cell count (WBC) were measured in conjunction with pain evaluation using visual analogue scale (VAS) before and after the trials. Result: HbA1c decreased significantly for patients on both trials. The magnitude of pain relief in the rehabilitating patients with HbA1c reduction more than 0.6% was ~3 times greater than those patients with less HbA1c reduction. However, no significant group difference in the pain relief was found between the conventional rehabilitation and rehabilitation with insulin administration. Both therapeutic methods did not significantly change inflammatory markers hsCRP and WBC following the 3-months interventions. Conclusion: The present study found greater pain relief efficacy after rehabilitation for those patients with better glycemic control.

碩士論文原創聲明書........................................ii
碩士學位考試審定書........................................iii
中文摘要................................................................iv
Abstract................................................................v
致謝....................................................................vi
目錄....................................................................vii
表目錄..................................................................ix
圖目錄..................................................................x
第壹章 緒論.........................................................1
第一節 研究背景................................................1
第二節　研究重要性.............................................2
第三節　研究目的...............................................3
第貳章 文獻探討................................................4
第一節 身體內的糖化現象.....................................4
第二節 RAGE與發炎反應......................................4
第三節 RAGE引起發炎的機轉.............................5
第四節 如何抑制RAGE引起的發炎反應.............6
第參章 研究方法....................................................8
第一節 受試者......................................................8
第二節 實驗設計....................................................9
第三節 分析方法....................................................10
第肆章 研究結果....................................................12
第伍章 討論.........................................................13
第一節 本實驗的主要發現....................................13
第二節 血糖值的高低與疼痛的相關性...................13
第三節 血糖值的高低與發炎反應的相關性...........14
第四節 積極調整血糖值的意義...............................16
第五節 調整血糖值與治療疼痛的意義.....................18
第陸章 結論...............................................................20
參考文獻..................................................................21
圖表說明..................................................................24
圖表..........................................................................26
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中文部分
鄧富元、龔素芳、夏毅然、高文斌、謝耀東（民95）。NF-κB在發炎反應、細胞凋亡與癌症生成過程中的調控。中華牙誌、25(1)、12-24.

英文部分
Cecil, D. L., Johnson, K., Rediske, J., Lotz, M., Schmidt, A. M., & Terkeltaub, R. (2005). Infalmmation-induced chondrocyte hypertrophy is driven by receptor for advanced Glycation end products. The Journal of Immunology, 175(12), 8296-8302.
Geroldi, D., Falcone, C., & Emanuele, E. (2006). Soluble receptor for advanced glycation end products: from disease marker to potential therapeutic target. Current Medicinal Chemistry, 13(17), 1971-1978.
Hoff, O. M., Midthjell, K., Zwart, J. A., & Hagen, K. (2008). The association between diabetes mellitus, glucose, and chronic musculoskeletal complaints, Result from the Nord-Trondelag health Study. BMC Musculoskeletal Disorders, 9, 160-167.
Hofmann, M.A., Drury, S., Hudson, B.I., Gleason, M.R., Qu, W., Lu, Y., et al. (2002). RAGE and arthritis:the G82S polymorphism amplifies the inflammatory response. Genes & Immunity, 3(3), 123-35.
Maillard-Lefebvre, H., Boulanger, E., Daroux, M., Gaxatte, C., Hudson, B.I.,& Lambert, M. (2009). Soluble receptor for advanced glycation end products: a new biomarker in diagnosis and prognosis of chronic inflammatory diseases. Rhemmatology, 48(10), 1190-1196.
Moser, B., Herold, K. C., & Schmidt, A. M. (2006). Receptor for advanced glycation end products and its ligand: initiators or amplifiers of joint inflammation-a bit of both? Arthritis & Rheumatism, 54(1), 14-18.
Pan,W. H., Yeh,W. T., Chan,H. Y., Hwu,C. M., & Ho, L. T. (2003). Prevalence and awareness of diabetes and mean fasting glucose by age, sex, and region: results from the Nutrition and Health Survey in Taiwan, 1993-1996. Diabetic Medicine, 20(3), 182-185
Puenpatom, R. A., & Victor, T. W. (2009). Increased prevalence of metabolic syndrome in individuals with osteoarthritis. Postgraduate Medicine, 121(6), 9-20
Pullerits, R., Brissier, M., Jonsson, I. M., & Tarkowski, A. (2006). Soluble receptor for advanced glycation end products triggers a proinflammatory cytokines cascade via bea 2 integrin Mac-1. Arthritis Rheumatism, 54(3), 898-907.
Ramchurn, N., Mashamba, C., Leitch, E., Arutchelvam, V., Narayanan, K., Weaver, J.,et al. (2009). Upper limb musculoskeletal abnormalities and poor metabolic control in diabetes. European Journal of Internal Medicine, 20(7), 718-721.
Retnakaran, R., Yakubovich, N., Qi,Y., Opsteen, C.,&Zinman, B. (2009). The response to short-term intensive insulin therapy in type 2 diabetes. Diabetes, Obesity and Metabolism, 27(5), 1028-1032.
Shih, S. (2009). The effects of Aging on glucose metabolism. Taiwan Geriatrics & Gerontrology, 4(1), 27-38.
Thye-Rønn, P., Sindrup, S. H., Arendt-Nielsen, L., Brennum, J., Hother-Nielsen, O., & Beck-Nielsen, H. (1994). Effect of short-term hyperglycemia per se on nociceptive and non-nociceptive thresholds. Pain, 56(1), 43-49.
Tighe, C. B., & Oakley, W. S. (2008). The prevalence of a diabetic condition and
adhesive causalities of the shoulder. Southern Medical Journal, 101(6), 591-595.
Vinik, A. (2007). Advancing Therapy in Type 2 Diabetes Mellitus with Early, Comprehensive Progression from Oral Agents to Insulin Therapy. Clinical Therapeutics, 29(6), 1236-1253.
Yao, D., & Brownlee, M. (2010). Hyperglycemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands. Diabetes, 59(1), 249-255.